Physiological mechanisms by which non-nutritive sweeteners may impact body weight and metabolism

Burke, Mary V.; Small, Dana M.

doi:10.1016/j.physbeh.2015.05.036

Cited by 114 publications

(108 citation statements)

References 133 publications

(126 reference statements)

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“…It was previously thought that the observed increase in appetite was due to the fact that artificial sweeteners did not activate the food reward pathways in the same way as sucrose and fructose (Yang 2010), perhaps resulting in compensatory overeating (Lavin et al 1997; Davidson et al 2011; Swithers et al 2013). However, recent evidence indicates that artificial sweeteners, specifically ASP, may have a direct effect on the gut microbiota that could explain the metabolic changes that occur in high-dose consumption of artificial sweeteners (Palmnas et al 2014; Suez et al 2014; Burke and Small 2015). …”

Section: Discussionmentioning

confidence: 99%

Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice

Gul

Hamilton

Munoz

et al. 2017

Appl. Physiol. Nutr. Metab.

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Diet soda consumption has not been associated with tangible weight loss. Aspartame (ASP) commonly substitutes sugar and one of its breakdown products is phenylalanine (PHE), a known inhibitor of intestinal alkaline phosphatase (IAP), a gut enzyme shown to prevent metabolic syndrome in mice. We hypothesized that ASP consumption might contribute to the development of metabolic syndrome based on PHE’s inhibition of endogenous IAP. The design of the study was such that for the in vitro model, IAP was added to diet and regular soda, and IAP activity was measured. For the acute model, a closed bowel loop was created in mice. ASP or water was instilled into it and IAP activity was measured. For the chronic model, mice were fed chow or high-fat diet (HFD) with/without ASP in the drinking water for 18 weeks. The results were that for the in vitro study, IAP activity was lower (p < 0.05) in solutions containing ASP compared with controls. For the acute model, endogenous IAP activity was reduced by 50% in the ASP group compared with controls (0.2 ± 0.03 vs 0.4 ± 0.24) (p = 0.02). For the chronic model, mice in the HFD + ASP group gained more weight compared with the HFD + water group (48.1 ± 1.6 vs 42.4 ± 3.1, p = 0.0001). Significant difference in glucose intolerance between the HFD ± ASP groups (53 913 ± 4000.58 (mg·min)/dL vs 42 003.75 ± 5331.61 (mg·min)/dL, respectively, p = 0.02). Fasting glucose and serum tumor necrosis factor-alpha levels were significantly higher in the HFD + ASP group (1.23- and 0.87-fold increases, respectively, p = 0.006 and p = 0.01). In conclusion, endogenous IAP’s protective effects in regard to the metabolic syndrome may be inhibited by PHE, a metabolite of ASP, perhaps explaining the lack of expected weight loss and metabolic improvements associated with diet drinks.

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Section: Discussionmentioning

confidence: 99%

Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice

Gul

Hamilton

Munoz

et al. 2017

Appl. Physiol. Nutr. Metab.

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show abstract

“…Moreover, according to according to Gardner et al (2012) nonnutritive sweeteners could facilitate reductions in added sugar intake and weight loss/control, promoting beneficial effects on related metabolic parameters. However there is still controversy regarding the harmful effects of consuming some sweeteners, mainly in relation to the use of artificial sweeteners (Fitch & Keim, 2012;Suez et al 2014;Burke & Small, 2015;Pepini, 2015;Hu, 2013). Moreover, Suez et al (2014) demonstrate that consumption of commonly used non-caloric artificial sweetener formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota.…”

Section: Introductionmentioning

confidence: 99%

Miracle fruit: An alternative sugar substitute in sour beverages

et al. 2016

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“…This effect of neuroprotection could be due to polar compounds obtained during the extraction of compounds like chlorophylls, carotenoids, phenolic and flavonoids involved in stevia and splenda. These substances are not physiologically inert compounds and their consumption may have potential biological mechanisms which may impact on energy balance and metabolic function (36). Ca 2+ , Mg 2+ ATPase activity increased in cortex and striatum regions, and decreased in cerebellum/medulla oblongata of animals that received sweeteners and cytarabine.…”

Section: Biochemical and Histological Changes Produced By Sweeteners mentioning

confidence: 99%

Biochemical and histological changes produced by sweeteners and cytarabine in the brain of young rats

García¹,

Brizuela²,

Peraza³

et al. 2018

Nutr Hosp

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Biochemical and histological changes produced by sweeteners and cytarabine in the brain of young rats Cambios bioquímicos e histológicos producidos por edulcorantes y citarabina en el cerebro de ratas jóvenes ResumenObjetivo: el objetivo fue evaluar el efecto de edulcorantes (splenda y stevia) sobre los niveles de dopamina, acido 5-hidroxiindolacetico (HIAA) y algunos biomarcadores de estrés oxidativo en presencia de citarabina. Métodos: cuarenta y ocho ratas Wistar machos con un peso aproximado de 80 g (cuatro semanas de edad), distribuidas en seis grupos de ocho animales cada uno, fueron tratados como sigue: grupo 1, control (NaCl 0,9% vehículo); grupo 2, citarabina (0,6 g/kg); grupo 3, stevia (0,6 g/kg); grupo 4, citarabina + stevia; grupo 5, splenda; y el grupo 6, citarabina + splenda. La citarabina fue administrada por vía intravenosa y la stevia y la splenda, por vía oral durante cinco días, utilizando una sonda orogástrica. Al final del tratamiento, los animales fueron sacrificados y se midieron los niveles de glucosa en sangre. Los cerebros fueron disecados para su análisis histológico y homogenizados para medir los niveles de dopamina, peroxidación lipídica (TBARS), metabolito de la serotonina (5-HIAA), actividad de la Na + , K + ATPasa y glutatión (GSH), usando métodos validados.Resultados: los edulcorantes aumentaron la glucosa en los animales que recibieron citarabina. La dopamina aumentó en la corteza y disminuyó en el estriado de los animales que recibieron stevia sola y combinada con citarabina. La 5-HIAA disminuyó en el estriado y el cerebelo/ médula oblongata de animales que recibieron edulcorantes y citarabina sola o combinada. El GSH se incrementó en los animales que recibieron edulcorantes. La lipoperoxidación disminuyó en los grupos que recibieron edulcorantes y citarabina. Estudios histopatológicos revelaron una degeneración neuronal importante en animales tratados con citarabina. Conclusión: los resultados muestran que los edulcorantes como stevia o splenda pueden conducir a la aparición de cambios desfavorables en los niveles de dopamina y 5-HIAA. Los cambios histológicos revelaron, además, lesiones marcadas de células neuronales en animales tratados con citarabina. AbstractObjective: The aim of this study was to evaluate the effect of splenda and stevia on dopamine and 5-HIAA levels, and some biomarkers of oxidative stress in the presence of cytarabine. Methods: Forty-eight young male Wistar rats each with a weight of 80 g (four weeks of age), distributed in six groups of eight animals each, were treated as follows: group 1, control (NaCl 0.9% vehicle); group 2, cytarabine (0.6 g/kg); group 3, stevia (0.6 g/kg); group 4, cytarabine + stevia; group 5, splenda; and group 6, cytarabine + splenda. Cytarabine was given intravenously (IV) while stevia and splenda were administered orally for five days, using orogastric tube. At the end of treatment, the animals were sacrificed and glucose levels in blood were measured. The brains were dissected for histological analysis and homogenated to mea...

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Physiological mechanisms by which non-nutritive sweeteners may impact body weight and metabolism

Cited by 114 publications

References 133 publications

Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice

Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice

Miracle fruit: An alternative sugar substitute in sour beverages

Biochemical and histological changes produced by sweeteners and cytarabine in the brain of young rats

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